Cross-pathway control

The photophysics and photochemistry of Ru(II) complexes have been extensively studied and good reviews are av able on this subject [1,86,87]. The type of reactivity associated with Ru(II) polypyridyl complexes in the excited state depends on the nature of this excited state and consequently on the different possible photophysical pathways controlling the luminescence lifetimes. For most polypyridyl Ru(II) complexes (for example Ru(bpy), Rufphenls", Ru(bpz)3. .. Fig. 2) [1, 86, 87], population of the excited singlet MLCT state is followed by crossing to the triplet MLCT state ( MLCT) with a quantum yield... 

Fig. 6. The gibberellin biosynthetic pathway in Zea mays shoots. The position in the pathway controlled by each of the dwarf mutants, dh d2, d2, and d5. is shown by a cross line on the appropriate arrow. This early-13-hydroxylation pathway leads to GA,. the bioactive GA controlling shoot elongation in maize. The absence of G A,. G A-,. and G A.. in the dl mutant, together with the accumulation of GA., [6]. suggest that the dl gene controls a common step leading to GA, and GA-,...

Air pollutants may enter plant systems by either a primary or a secondary pathway. The primary pathway is analogous to human inhalation. Figure 8-2 shows the cross section of a leaf. Both of the outer surfaces are covered by a layer of epidermal cells, which help in moisture retention. Between the epidermal layers are the mesophyll cells—the spongy and palisade parenchyma. The leaf has a vascular bundle which carries water, minerals, and carbohydrates throughout the plant. Two important features shown in Fig. 8-2 are the openings in the epidermal layers called stomates, which are controlled by guard cells which can open and close, and air spaces in the interior of the leaf. 

Moreover, the CSN is involved in checkpoint control. The double deletions of csnl and csn2 mutants crossed with checkpoint pathway mutants such as rad3, chk, and cdsl are synthetically lethal in S. pombe [52]. Cdsl kinase is constitutively activated in csnl mutants. Similarly, loss of csn5 in Drosophila results in activation of Mei-41, one of the ATM/ATR family kinases involved in meiotic checkpoint upon DNA damage [90]. 

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